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Updated: Mar 24, 2026

Examining the Dynamics of Cellular Adhesion and Spreading of Epithelial Cells on Fibronectin During Oxidative Stress
Published on: October 13, 2019
Fibronectin Modulates Cell Adhesion and Signaling to Promote Single Cell Migration of Highly Invasive Oral Squamous
Grasieli de Oliveira Ramos1,2, Lisiane Bernardi1, Isabel Lauxen1
1Basic Research Center, Dentistry School, Federal University of Rio Grande of Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Extracellular matrix (ECM) components influence oral cancer cell migration. Fibronectin promotes invasive single-cell movement in aggressive tumors, while laminin supports collective migration in less invasive ones.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Cell migration is crucial for cancer invasion and metastasis.
- Integrins and RhoGTPases regulate cell adhesion and actomyosin organization.
- Tumor cells encounter diverse extracellular matrix (ECM) components during invasion.
Purpose of the Study:
- To investigate how ECM composition affects the invasiveness of Oral Squamous Cell Carcinoma (OSCC).
- To determine the role of fibronectin and laminin in OSCC cell migration and invasion.
Main Methods:
- Culturing two OSCC lines with differing invasiveness (Linv/HE-cad and Hinv/LE-cad) on various ECM components.
- Analyzing migratory properties, cell adhesion, and RhoGTPase (RhoA, Rac1) activity.
- Examining human OSCC biopsies for cell-ECM adhesion patterns.
Main Results:
- Fibronectin induced non-directional collective migration and decreased RhoA activity in low-invasive OSCC.
- In highly invasive OSCC, fibronectin increased Rac1 activity and promoted fast single-cell migration.
- OSCC biopsies showed similar ECM adhesion changes at the tumor invasive front.
Conclusions:
- ECM composition, particularly fibronectin, can dictate OSCC invasiveness by switching migration modes.
- Changes in cell-ECM adhesion and downstream signaling pathways alter actomyosin organization, influencing collective vs. single-cell migration.
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